Combined Open-Angle and Angle-Closure Glaucoma
David L. Epstein, MD, MMM; Ari D. Schuman, MD, MS; and Joel S. Schuman, MD, FACS
The obstruction to aqueous outflow in primary open-angle glaucoma is due mainly to abnormalities within or just beyond the trabecular meshwork (TM), whereas in angle-closure glaucoma the cause of obstruction to aqueous outflow is contact between the periphery of the iris and the corneoscleral TM, preventing access of aqueous humor to the normal aqueous outflow system. There is no reason why both conditions could not occur in the same eye. Because each has an independent basis, a certain number of coincidences of this sort can be expected.1 On the other hand, there are more cases of “residual open-angle glaucoma” after laser iridectomy than would be expected by chance (see Chapter 56).
There is also a hypothetical possibility that repeated episodes of angle closure could cause permanent damage to the corneoscleral TM even without formation of peripheral anterior synechiae, and that they could in this way induce a form of permanent open-angle glaucoma, which would persist between episodes of angle closure and after angle-closure attacks were terminated by iridectomy. This has been mentioned previously (open-angle glaucoma due to chronic iris touch in Chapter 23). As yet, however, we lack clear evidence for this mechanism.
Occasionally, patients present evidence of having both open-angle and angle-closure glaucoma. In some of these patients, one may be certain that only 2, 3, or 4 hours of the angle are closed, but one may find an intraocular pressure (IOP) of 40 mm Hg, and tonography may indicate an impairment of facility of outflow consistent with the IOP, but disproportionately more than the extent of angle closure. When the findings are this clear and definitive, the diagnosis is easy. One has to conclude that there is not enough angle closure to account for this amount of glaucoma.
In many other cases, it is much more difficult to establish whether one is dealing with pure angle-closure glaucoma or a combination of angle-closure with open-angle glaucoma. Difficulty in establishing a definite diagnosis of combined open-angle and angle-closure glaucoma, or of distinguishing between open-angle and angle-closure glaucoma, is greatest when a question of chronic appositional angle closure is involved. The other varieties of angle closure seldom present a problem in this regard. For instance, in acute angle-closure glaucoma, when all the typical symptoms and signs are present, we are seldom confronted with glaucoma out of proportion to the extent of closure during an attack, or out of proportion to any residual peripheral anterior synechiae after iridectomy is done. Also, in chronic synechial angle-closure glaucoma in which a considerable portion of the angle has gradually become closed by synechiae, it is uncommon to find glaucoma out of proportion to the extent of angle closure, or residual glaucoma after iridectomy out of proportion to the extent of synechiae.
The greatest problem is encountered in eyes in which the angle is so narrow in a portion of the circumference that we think, but cannot be sure, that some of it is actually closed, while at the same time measurements of IOP and facility of outflow suggest that the glaucoma is more severe than would be expected from the conceivable extent of angle closure. When closure of only a portion of the circumference is in question, it may be very difficult to prove whether angle closure is actually taking place. If laser iridectomy is done in these cases, and the angle becomes widened so that we can rule out future episodes of angle closure, we may find that IOP and facility of outflow are not improved and that the open-angle glaucoma that is present requires continuing treatment. However, peripheral iridectomy in such cases confers the real benefit of eliminating concern about future attacks of angle-closure glaucoma. The benefit/risk ratio of laser iridectomy is such that it is often used to eliminate any angle-closure component. However, it is important to realize that surgical iridectomy was also previously so used. The following case illustrates this situation.
CASE 39-1
A man, aged 47 years with hypermetropia of 5 D, a history of hypermetropia in many relatives, and acute glaucoma in his hypermetropic grandfather, was referred to us because of extremely narrow angles in both eyes. Optic nerve heads and fields were normal.
We found applanation IOPs of 26 to 30 mm Hg on different occasions, and tonographic C value of 0.11, in both eyes. The anterior chambers were not excessively shallow axially (equivalent to 4 or 5 corneal thicknesses), but the irides were convex peripherally, and the angles appeared to be closed in one-third to one-half the circumference, very narrow in the remainder. Trial of 2% and later 4% pilocarpine in one eye did not improve the facility of outflow, but under this treatment IOP was 20 mm Hg; the angle remained so narrow that it was impossible to say whether the angle in the superior quadrant opened; in the rest of the circumference the angle was definitely open, but extremely narrow.
The tonographic measurements indicated more obstruction to aqueous outflow than would be explained by closure of a small fraction of the angle, so we concluded that the glaucoma was mainly of the open-angle variety, but because of the extreme narrowness of the angle and probably closure of a portion, peripheral iridectomy was performed on each eye as a protective measure.
Several months after the iridectomies, when the eyes were entirely healed and quiet, examination without treatment showed applanation IOPs of 25 mm Hg and tonographic C values of 0.12 in both eyes, all essentially the same as before the operation. The angles were only slightly less narrow than before iridectomy, but now discernibly open superiorly and definitely open in the rest of the circumference. A view obtained through the surgical colobomas suggested that the persistent narrowness of the angles might be attributable to the position of the ciliary processes, which were in contact with the back of the iris and appeared possibly to be holding the periphery of the iris forward. After iridectomy, the persistent narrowness of these angles clearly was not due to accumulation of aqueous in the posterior chamber.
We concluded that, as suspected preoperatively, the glaucoma in this patient was principally open-angle glaucoma but that the peripheral iridectomies had been worthwhile. Although the iridectomies caused only slight widening of the angles in this case, that amount appeared critical. Furthermore, by eliminating all hindrance to the flow of aqueous from posterior to anterior chamber, the iridectomies made safe and feasible the future use of all types of miotics and epinephrine-like drugs, which eventually may be needed for control of the open-angle glaucoma during the patient’s expected 30 or 40 remaining years of life.
As a principle of treatment, when the angle is extremely narrow, and especially when it is certain that a portion of the angle can close when the eye is without treatment, but there is conclusive evidence of open-angle glaucoma with the facility of outflow persistently subnormal when the angle is open, either spontaneously or under miotics, there is justification for performing laser iridectomy to eliminate the pupillary block angle-closure element and to permit use of all types of medication for the open-angle glaucoma. In eyes having open-angle glaucoma with a very narrow angle, which have developed acute angle-closure glaucoma, the status of the previously open-angle glaucoma is unchanged after iridectomy. The iridectomy is intended purely to prevent or relieve angle-closure glaucoma.
Eyes that have been under intensive treatment for open-angle glaucoma and have angles that are only moderately narrow, with full width of TM visible gonioscopically and not therefore threateningly narrow, and never having closed spontaneously, merit assessment by modified dark room testing. In such testing, the patient is scanned with ultrasound biomicroscopy under light room and darkened room conditions, and the relative state of the angle is assessed. A similar test can be done in a darkened examination room using slit-lamp gonioscopy. Should the angle close under dark conditions, the patient should undergo laser peripheral iridectomy.
Many of these issues have been discussed in Chapter 56, especially in terms of the indication for laser iridectomy and the categories of residual open-angle glaucoma after iridectomy. The physiological principles of correlating the extent of angle closure with the IOP elevation have been discussed in Chapters 3 and 7. In addition to these considerations of open-angle glaucoma in eyes with angle closure, the reverse category of a superimposed angle-closure component to a basic open-angle glaucoma process needs to be considered and has been discussed in Chapter 19. In particular, the occurrence of a subsequent additional angle-closure component to an open-angle glaucoma due to pseudoexfoliation2,3 needs to be kept in mind: it is not rare.
Patients with presumed primary open-angle glaucoma need periodic repeated gonioscopy and should always have gonioscopy when the IOP is elevated at a follow-up visit. In addition to identifying a superimposed angle-closure component, other causes, such as occult inflammatory precipitates or new blood vessels, need to be ruled out. When a patient with primary open-angle glaucoma seems to demonstrate some functional angle closure (usually 4 hours or more), but there is no peripheral anterior synechiae formation on indentation gonioscopy, and thus there is some uncertainty whether there is truly a functional appositional angle-closure component or whether the angle is narrow but still functionally open (see Chapter 28), the risk/benefit considerations are such that after fully informing the patient about these considerations as well as one’s diagnostic uncertainty (and what the clinician would do if it were his or her eye), it is usually wisest to proceed with laser iridectomy. This is because in this situation the risk of not treating a possible angle-closure glaucoma component is greater than the risk of the procedure.
Nevertheless, the clinician and the patient need to be fully prepared for an IOP spike that may be substantial if, for example, the glaucoma is entirely due to an open-angle pseudoexfoliation mechanism rather than some functional angle-closure component. In this situation, pigment and other iris debris from the iridectomy and inflammation may provide further short-term and possibly long-term insult to TM function. Regardless, the iridectomy may be indicated for prophylactic purposes, but the patient (and clinician) need to know ahead of time that the iridectomy will not improve the IOP in the short term and may cause a substantial acute IOP spike.
Finally, chronic silent angle closure may masquerade as “open-angle glaucoma” given the absence of symptoms, especially if gonioscopy is not performed.4,5
The usual aqueous suppressant therapy for such presumed open-angle glaucoma, by decreasing the vectors acting on the posterior iris surface, may somewhat deepen the angle perpetuating the misdiagnosis (see Chapter 13). Such an action needs to be evaluated in any patient suspected of having combined mechanism glaucoma.
REFERENCES
1. Hyams SW, Keroub C, Pokotilo E. Mixed glaucoma. Br J Ophthalmol. 1977;61(2):105-106.
2. Gross FJ, Tingey D, Epstein DL. Increased prevalence of occludable angles and angle-closure glaucoma in patients with pseudoexfoliation. Am J Ophthalmol. 1993;117:333-336.
3. Varma DK, Simpson SM, Rai AS, et al. Undetected angle closure in patients with a diagnosis of open-angle glaucoma. Can J Ophthalmol. 2017;52(4):373-378.
4. Coleman AL, Yu F, Evans SJ. Use of gonioscopy in medicare beneficiaries before glaucoma surgery. J Glaucoma. 2006;15(6):486-493.
5. Cassard SD, Quigley HA, Gower EW, et al. Regional variations and trends in the prevalence of diagnosed glaucoma in the Medicare population. Ophthalmology. 2012;119(7):1342-1351.
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